Journal of Current Medical Research and Opinion Received 16-09-2020 | Accepted 10-10-2020 | Published Online 11--10-2020

DOI: https://doi.org/10.15520/jcmro.v3i10.351 ISSN (O) 2589-8779 | (P) 2589-8760 CMRO 11 (10), 652−664 (2020)

REVIEW ARTICLE

Disease of and Periradicular Tissue: An Overview

∗ Geetanjali Singh1 Sanjana Paul R2 Ayush Arora3 Shakti Kumar4 Lucky Jindal5 Sachin Raina6

1Senior Lecturer, Department of Abstract: Prosthodontics, , Bridge Dental pain is the most common reason due to which patient seek dental and Implantology, Himachal treatment. Pain occur due to diseases involving pulp and periradicular Dental College, Sundernagar, Himachal Pradesh tissues, as these tissues are richly innervated and have ample of blood supply. Also it is enclosed by surrounding tissues that are incapable 2Consultant Endodontist, Kanyakumari, Tamil Nadu of expanding, such as dentin and also has terminal blood flow and small-gauge circulatory access the periapex. All of these characteristics 3Consultant Dental Surgeon, severely constrain the defensive capacity of the pulp tissue when faced Jaipur, Rajasthan with the different aggressions it may be subjected to. In addition to above mentioned characterstics, pulp tissue can also be affected by a 4Consultant Orthodontist, Sirsa, Haryana retrograde infection, arising from the secondary canaliculi, from the periodontal ligament or from the apex during the course of periodontitis. 5Senior Lecturer, Department of Paedodontics and Preventive this review article basically concentrates on structure of pulp, classifi- Dentistry, JCD Dental College, cation of diseases related to pulp and periradicular tissue and detailed Sirsa, Haryana explanation of diseases. 6Intern, Himachal Institute of Dental Sciences, Paonta Sahib, Keywords: Abscess, Periodontitis, Pulp, Himachal Pradesh

1 INTRODUCTION

Supplementary information The online version of ulp has been described as a highly resistant this article (https://doi.org/10.15520/jcmro.v3i10.35 organ and sometime as an organ with little 1) contains supplementary material, which is avail- Por no resistance as its resistance depends on able to authorized users. cellular activity, nutritional supply, age and other metabolic and physiologic parameters. (1) The dental Corresponding Author: Geetanjali Singh Senior Lecturer, Department of Prosthodontics, Crown, pulp consists of vascular connective tissue contained Bridge and Implantology, Himachal Dental College, within rigid dentin walls. (2) It is the principal source Sundernagar, Himachal Pradesh of pain within the mouth and also the major site of at- Email: [email protected] tention in and restorative treatment. (3)

CMRO 11 (10), 652−664 CURRENT MEDICAL RESEARCH AND OPINION 652 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION

Stimuli----> deposition of secondary dentin ----> reducing size of pulp chamber and volume-----> • Diagnostic method by – Tooth may disclose an enamel crack which may be better visualized by reduces the cellular, vascular and neural content of using a dye or transilluminating the tooth with the pulp results in atrophy (3) fibre optic light 2 DISCUSSION • Treatment-a full crown restoration immobilis- The first and foremost reaction of pulp tissue to ing the fragments. irritation is “Inflammation”, but the basic disease process that is involved in pulp and periapical disease is “Infection”. Infection can start from pulp and spread to periodontal tissue and vice versa is also occuring at low atmospheric pressure. possible. (4) It occurs in high altitude. For example, in chronic Causes of Pulp Disease (5, 6) disease no symptoms occur at ground level but at high altitude pain occurs due to low atmospheric • Physical pressure. b) Thermal a) Mechanical 1. Trauma • Heat from cavity preparation , at either low or high speed A. Accidental (contact sports) – traumatic injury to pulp due to violent blow to the tooth during a • If there are deep fillings without protective base fight, sports or household accidents. Habits such as there will be conduction of heat. opening booby pins with the teeth and nail biting may also cause pulp injury. • Polishing of restoration will lead to production B. Iatrogenic dental procedures such as of frictional Heat

• during excavation of carious tooth structure, c) Chemical cause- there might be accidental exposure of the pulp • Phosphoric acid and acrylic monomer etc. • Rapid movement of teeth by means of mechan- ical separator and during orthodontic treatment • Erosion by acids

• The use of pins for mechanical retention of amalgam. d) Infection caused by bacteria and their by products enter pulp through- 2.Pathologic wear – , etc

3.Crack tooth syndrome • Caries associated toxins. 4.Barodontalgia Crack Tooth Syndrome • Direct invasion of the pulp from caries or trauma

• Incomplete fractures through the body of tooth. • Microbial colonization in pulp by blood borne micro organisms (anachoresis) • Symptom – pain ranging from mild to excrutiat- ing, at the initiation or release of biting pressure • Entry of bacteria through developmental groove

CURRENT MEDICAL RESEARCH AND OPINION CMRO 11 (10), 652−664 (2020) 653 DISEASE OF PULP AND PERIRADICULAR TISSUE: AN OVERVIEW

TABLE 1: Fibers associtaed with dental pain a. Dentinal hypersenstivity. b. Hyperemia. 2. Acute pulpalgia. a. Incipient. b. Moderate. c. Advanced. 3. Chronic pulpalgia. 4. Hyperplastic pulpitis.

1. Necrotic pulp.

2. Internal resorption.

3. Traumatic occlusion.

4. Incomplete fracture

Classification (Weine) (10)

• Inflammatory changes Pulp fibres associated with dental pain have been describes in Table 1 (7) 1. Hyperplastic (reversible pulpitis). Classification of Diseases of Pulp According to Grossman (8) a. Hypersenstive dentin. b. Hyperemia • Inflammatory diseases of dental pulp 1. Acute pulpalgia (acute pulpitis) (a) Reversible pulpitis 1. Symptomatic (acute) 2. Chronic pulpalgia (subacute pulpitis) 2. Asymptomatic (chronic) 3. Chronic pulpitis (b) Irreversible pulpitis 4. Chronic hyperplastic pulpitis 1. Acute – 1 abnormally responsive to cold 2 abnormally responsive to heat 5. Pulp 2. Chronic -1 Asymptomatic with pulp exposure B. Retrogressive changes 2 Hyper plastic pulpitis 3 Internal resorption 1. Atrophy

1. Pulp degeneration- 1.calcific 2. atrophic 2. Dystropic calcifications

• Pulp necrosis Reversible Pulpitis (6, 10, 11) It is one of the earliest form of pulpitis and at one Classification (Ingles ) (9) time referred to as “pulp hyperaemia”. 1.Hyperreactive pulpalgia. Symptoms

CMRO 11 (10), 652−664 (2020) CURRENT MEDICAL RESEARCH AND OPINION 654 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION • The pulp is inflamed to the extent that thermal stimuli- usually cold- cause a quick, sharp, hy- Irreversible Pulpitis (6, 11) persensitive response that subsides as soon as Is a persistent inflammatory condition of the pulp, stimulus is removed– symptomatic reversible symptomatic or asymptomatic, caused by noxious pulpitis. stimulus. Pain occurs spontaneously and it persists • Pain is not spontaneous. Occurs due to stimula- for several min to hrs and lingers on even after tion of A delta nerve fibres. removal of stimulus. Early symptoms • If the irritant is removed by sealing the tubules, pulp will revert to asymptomatic. Or if the symptoms persist, it leads to irreversible pulpi- • Pain is sharp, piercing, shooting and may be tis. intermittent or continuous which occurs due to stimulation of C- fibres. • Asymptomatic reversible pulpitis In later stages Histopathology There is capillary bed engorgement with oedema — • Pain is so severe in later stages and can be —prolonged vasodilation———increased capillary described as boring, gnawing, or throbbing. Its pressure——–increased vascular permeability——– intensity is increased by heat and sometimes increased blood volume———increased intrapulpal relieved by cold. Patients often kept awake at pressure——pain occurs. night by pain.

Histopathology Diagnosis As decay reaches the pulp following changes are seen: • Pain short duration venules become congested causing necrosis— • Stimulus – required — necrosis attract PMN’s by chemotaxis—— -Acute inflammation——–phagocytosis———- • History - recent dental procedures PMN’s die ——-release lysozyme ———purulent • Percussion test - negative exudates———-microabcess is formed——pulp protects itself with fibrous connective tissue. • Referred pain - negative Microscopically, one sees the area of abscess, zone • On lying down pain - negative of necrotic tissue, with micro organisms present in the late carious state, along with lymphocytes, • Color change - negative plasma cells, .

• Radiograph - normal Diagnosis • Vitality test - cold intensifies pain • Pain-Continuous &throbbing Treatment Prevention is best treatment .Periodic care is done to • Stimulus-Not required , spontaneous pain prevent development of caries. Use of cavity varnish • History-Deep caries, trauma , extensive restora- or base followed by proper filling and polishing. If tion pain persists even after removal of stimulus irre- versible pulpitis occurs- treated by pulp extirpation. • Percussion test-Positive

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• Referred pain-Positive It is an idiopathic slow or fast progressive resorptive process occurring in the dentin of pulp chamber or • On lying down pain-positive root canals of tooth. It is painless condition stimu- lated by trauma which produces dentin destruction. • Color -Positive due to tissue lysis Tooth is asymptomatic but on perforation of root • Radiograph-Widening of PDL space pain occurs. Appearance: Pink Spot • Vitality test-Heat intensifies pain cold relieves pain Histopathology Treatment It is the result of osteoclastic activity. The resorptive Complete removal of the pulp or pulpectomy and process is characterized by lacunae, which may be surgical removal is considered if tooth is not filled in by osteoid tissue and presence of granulation restorable. tissue accounts for profuse bleeding when the pulp is removed. Multinucleated giant cells are usually seen Chronic Hyperplastic Pulpitis (Pulp Polyp) (12–14) when pulp is chronically inflamed. Diagnosis • A reddish cauliflower like growth of pulp tissue through & around a carious exposure of young Radiographic features pulp characterized by development of granula- tion tissue • Radiographically appears as uniform, round or ovoid radiolucent enlargement of pulp chamber

Histopathology • It does not involve the bone , if perforation Microscopically, a complex of new capillaries, pro- occurs the bone adjacent to it is resorbed liferating fibroblasts and inflammatory cells are present in pulp polyp. The tissue in the pulp chamber is often transformed into granulation tissue, which Vitality test: occurs in teeth with vital pulps &give projects from the pulp into the carious lesion. positive response to sensitivity tests. Diagnosis Treatment Pulp extirpation stops the internal resorption, after • If hyperplastic tissue grow beyond the cavity of repair defect is obturated with plasticized gutta per- tooth, it appears as if gum is growing into the cha. cavity. Differentiate it by raising the tissue back to its origin. Pulp Degeneration (18) Generally present in older people. It may be the result • Radiograph shows large open cavity with direct of persistent, mild irritation. May also be induced by access to pulp chamber. attrition, abrasion, erosion, bacteria etc. It occurs in 2 forms Differential Diagnosis It should be differentially diagnosed from gum polyp 1. Calcific degeneration by raising the stalk back to its origin. 2. Atrophic degeneration Treatment Elimination of polypoid tissue, removal of pulp fol- Calcific Degeneration: It occur when part of pulp lowed by restoration. tissue is replaced by calcific material i.e pulp stones Internal Resorption (10, 15–17) (denticles)

CMRO 11 (10), 652−664 (2020) CURRENT MEDICAL RESEARCH AND OPINION 656 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION Pulp stones are classified as – Symptoms: Discoloration of tooth, no painful symp- a) according to location - 1) free 2) embedded 3) toms occur attached Diagnosis b) according to structure- 1) true 2 )false True Denticles • Radiographic changes – shows large cavity & thickening of PDL. Made up of localized mass of calcified tissue that resemble dentin because of their tubular structure, • Vitality test – tooth is not responding to vitality more common in pulp chamber than in root canal and test nodules bear great resemblance to secondary dentin. False Denticles • Visual examination: due to lack of normal translucency tooth appear opaque . Localised mass of calcified tissue, does not exhibit tubular structure. Nodules appear to be made up • Histopathology – inflammation is seen. of concentric layers or lamellae deposited around a central nidus. More common in pulp chamber than Treatment in root canal. Free Denticles • or extraction in non Denticles lying entirely within the pulp chamber and restorable tooth. not attached to dentin walls Attached Denticles Diseases of Periradicular Tissue Denticles lying within the pulp chamber and is con- Pulpal diseases are one of the most common cause of tinuous with the dentin walls periradicular diseases, as there is inter relationship Radiographically, appears as intracanal radiopacity between pulp and periradicular tissues through the similar to surrounding dentin. Calcific degeneration various foramina of root canals and give rise to of complete pulp space occurs as a sequale to trau- inflammatory and immunologic reactions through matic injury is known as Calcific Metamorphosis the passage of bacterial products and toxins. It is said that even pulpal inflammation causes inflammatory Atrophic Degeneration changes in the periodontal ligament even before pulp Decrease in size occurs slowly as tooth grows old. becomes totally necrotic. (20) Fewer stellate cells are present &intracellular fluid Classification is increased. Replacement of cellular elements with fibrous tissue is called as fibrous degeneration. (10) According to Grossman (8) Pulp Necrosis (19) 1. Acute periradicular diseases Necrosis is death of pulp. (A) Acute apical periodontitis Types (B) Acute alveolar abcess (C) Acute exacerbation of chronic apical periodonti- • In Coagulation necrosis soluble part of tissue is tis converted into solid material 2. Chronic periradicular diseases • Caseation (A) Chronic apical periodontitis (a) Chronic alveolar abcess • Liquefaction necrosis (b) Cystic apical periodontitis Cause: Noxious insult or injury to pulp such as (B) Persistent apical periodontitis trauma, bacteria, chemical irritation. 3. Condensing osteitis

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4. External root resorption Classification (Weine) (10) 5. Diseases of periradicular tissue of non endodontic i) Apical periodontitis origin -Acute apical periodontitis (AAP) Classification (Ingles) (9) -Chronic apical periodontitis( CAP) Periradicular lesions are divided into three main - Condensing ostetitis clinical groups. ii) Apical abscess a) Symptomatic (acute) apical periodontitis (SAP) - Acute apical abscess (AAP) b) Asymptomatic (chronic) apical periodontitis (AAP) -Chronic apical abscess (CAP) i) Periapical granuloma iii) Non-endodontic periapical lesions ii) periradicular cyst iii) condensing osteitis - c) Apical abscess -Lateral periodontal cyst i) Symptomatic Apical Abscess -Odontogenic keratocyst ii) Asymptomatic Apical Abscess -Residual apical cyst Non-Endodontic Periradicular Lesions Odontogenic tumor Odontogenic Cysts Non-Odontogenic tumor . Routes of Micro-organism Ingress • Dentigerous cyst Through the open cavity, dentinal tubules, gingival • Lateral periodontal cyst sulcus, periodontal ligament, blood stream, broken occlusal seal or faulty restoration of a tooth pre- • Odontogenic keratocyst viously treated by endodontic therapy and exten- sion of a periapical infection from adjacent infected • Residual apical cyst teeth. (20) Bone : fibrous- osseous lesions Acute Apical Periodontitis (21, 22) Painful inflammation around the apex as an exten- • Periradicular cemental dysplasia sion of pulpal inflammation into periapical tissue, mechanical or chemical trauma by endodontic in- • Osteoblastoma & cementoblastoma struments or materials or caused by • Cementifying & Ossifying fibroma hyperocclusion or bruxism. Causes Odontogenic Tumor 1. Abnormal occlusal contacts - Ameloblastoma 2. Recently inserted restoration extending beyond the Non-Odontogenic Lesions occlusal plane. 3. Traumatic blow to the tooth • Central giant cell granuloma 4. Bacterial or noxious products from an inflamed, • Nasopalatine duct cyst necrotic pulp 5. over instrumentation during cleaning and shaping • Simple root canal • Globulomaxillary cyst 6. Forcing of irritants through the apical foramen

CMRO 11 (10), 652−664 (2020) CURRENT MEDICAL RESEARCH AND OPINION 658 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION 7. Extension of obturating material through the apical • Osteitis, periostitis, cellulites or osteomyelitis foramen. may occur if left unattended.

Symptoms • Sinus tract is formed usually on labial and buc- Patient complains of pain on closure and mastication cal mucosa though which pus drainage occur. and tenderness of tooth. Tooth may feel slightly sore and extruded. Diagnosis Histopathology • Generally made quick and accurately from the • An inflammatory reaction occurs in the PDL. clinical examination and from the subjective history give by the patient. • Dilatation of blood vessels, PMN’s are present, and an accumulation of serous exudates dis- • A radiograph may help one to determine the tends the PDL and extrudes the tooth slightly. tooth affected by showing a cavity, a defective restoration, thickened PDL space, or evidence • Severe irritation lead to activation of osteoclast of breakdown of bone. resulting in breakdown of periradicular bone, and the acute alveolar abscess may follows • Affected tooth may be tender to percussion or patient may state that it hurts to chew with the Diagnosis tooth. • Apical mucosa tender on palpation and tooth • Tender on percussion is classical diagnostic fea- may be mobile and extruded. ture. Radiographically thickening of PDL or a small area of rarefaction is present. Histopathology

Treatment: Occlusal adjustement and removal of • The marked infiltration of PMN’S and the rapid irritants is the immediate line of the treatment accumulation of inflammatory exudates in re- Acute Alveolar Abcess (20, 23, 24) sponse to an active infection distend the PDL Localised collection of the pus in the alveolar bone & there by elongate the tooth. If the process at the root apex of the tooth from the necrotic pulp, continue, periodontal fibers will separate. with extension of infection through apical foramen • Although some mononuclear cells may be into periradicular tissues. found, the chief inflammatory cells are PMN’S. Causes • As the bony tissue in the region of the root apex • Trauma or of chemical or mechanical irritation. is resorbed, and as more and more of the PMN’S die in their battle with the microorganisms, pus • The immediate cause is generally bacterial in- is formed. vasion of dead pulp tissues • Microscopically, one sees an empty space or Symptoms spaces, where suppuration has occurred, sur- rounded by PMN’S & some mononuclear cells. • Tenderness is the first symptom felt which is re- lieved by continous slight pressure on extruded Treatment tooth to push it back into the alveolus. • The immediate treatment consists of establish- • Later severe, throbbing pain occur with atten- ing the drainage and controlling the systemic dant swelling of the overlying soft tissue. reaction.

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Acute Excacerbation of • The exacerbation associated with the initiation (Phoenix Abcess) (25) of root canal therapy in a completely asymp- An acute periapical exacerbation that arises from a tomatic tooth. previously existing chronic lesion. • In such a tooth, radiographs show well-defined Cause periradicular lesion. • The patient may have a history of a traumatic 1. Noxious stimuli from a diseased pulp with accident that turned the tooth dark after a period chronic periradicular disease. of time or of postoperative pain in a tooth that 2. While chronic periradicular diseases, Such as had subsided until the present episode of pain. granulomas and cysts, are in a state of equilib- • Lack of response to vitality tests points to a rium, these apical reactions can be completely diagnosis of necrotic pulp. asymptomatic. Treatment 3. At times, because of an influx of necrotic prod- ucts from a diseased pulp, or because of bac- • Establishing drainage and controlling of sys- teria and their toxins, these apparently dormant temic reaction. lesions may react and may cause an acute in- flammatory response. Periapical Granuloma (26, 27) Dental granuloma is a granulomatus tissue continu- 4. Lowering of the body’s defenses in the presence ous with the PDL, resulting from death of the pulp of bacteria and the bacteria toxins released from & diffusion of bacteria and bacterial product toxins the root canal. from the root canal into the surrounding periradicular 5. Root canal instrumentation leads to mechanical tissues through the apical and lateral foramen. irritation that may also trigger an acute inflam- Inflamation in Dental Granuloma is misnomer. matory response. Because its tissue is chronic in nature & not a tu- mor. A granuloma contains “Granulomatous” tissue, Symptoms that is granulation tissue & chronic inflammatory in composition. A granuloma may be seen as a chronic • Tender on touch during initial stages. low grade defensive reaction of the alveolar bone to irritation from the root canal. • As inflammation progresses, the tooth may be Cause elevated in its socket and may become sensitive. • Death of pulp followed by mild infection or • The mucosa over the radicular area may be irritation of the periradicular tissue. sensitive to palpation and may appear red and swollen. • In some cases granuloma preceded by a chronic alveolar abscess. Histopathology • Experimental evidence has shown that a granu- In the granuloma or cyst and the adjacent periradic- loma is cell mediated response to pulpal bacte- ular tissues are areas of liquefaction necrosis with rial products. disintegrating polymorphonuclear neutrophils and cellular debris (pus).These areas are surrounded by Symptom infiltration of macrophages and some lymphocytes No subjective symptom, except in rare cases when it and breaks down & undergoes suppuration. Diagnosis Diagnosis

CMRO 11 (10), 652−664 (2020) CURRENT MEDICAL RESEARCH AND OPINION 660 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION • Generally discovered during routine radio- Radicular Cyst (28, 29) graphic examination. A radicular cyst is a cyst most likely results of • Area of rarefaction is well defined, with lack of epithelial cells (Malassez) in the periodontal liga- continuity of the lamina dura. ment are stimulated to proliferate and undergo cystic degeneration by inflammatory products from a non • Exact diagnosis can be made only by micro- vital tooth.The lumen of the cyst is filled with a low scopic examination. – concentration of proteinaceous fluid. ′ • Generally tooth non tender to percussion & it s Causes not loose. • Physical • Mucosa over the root may or may not tender on palpation • Chemical • A sinus tract may be present. Tooth does not • Bacterial respond to thermal or EPT. Symptoms • Patient may give a history of pulpalgia that sub sided • No symptoms are associated with the devel- opment of a cyst, except those incidentals to Histopathology necrosis of the pulp. Granulomatous tissue replaces the alveolar bone and PDL. • Tooth movement occur due to pressure of the cyst, owing to accumulation of cystic fluid. As It consists of a rich vascular net work, fibroblasts and a result the root apices of the involved teeth a moderate infiltration of lymphocytes and plasma become spread apart, so the crowns are forced cells. Macrophages and foreign – body giant cells out of alignment. may also be present. As the inflammatory reaction continues, because of • Tooth also become mobile. irritation from bacterial or their products, the exu- dates accumulates at the expense of the surrounding • If left untreated, cyst continue to grow at the alveolar bone, expense of the maxilla or the mandible. This process is followed by clearing of the dead osseous tissue by macrophages or foreign-body gi- ant cells while, at the periphery, fibroblasts actively build a fibrous wall. Diagnosis Some granulomas consist foam cells, macrophages containing lipid material, and cholesterol. The alve- • Tooth with a radicular cyst does not react to olar bone may show resorption and osteoclasts may electrical or thermal stimuli, and results of other be present. clinical tests are negative, except the radio- graph. The patient may report a previous history Treatment of pain. • Extraction of involved tooth • Usually, on radiographic examination, shows • Root canal therapy loss of continuity of the lamina dura with an area of rarefaction. The radiolucent area is generally • If left untreated, may undergo transformation round in outline, except where it approximates into an apical periodontal cyst through prolif- adjacent teeth, in which case it may be flattened eration of epithelial rests in the area. and may have on oval shape.

CURRENT MEDICAL RESEARCH AND OPINION CMRO 11 (10), 652−664 (2020) 661 DISEASE OF PULP AND PERIRADICULAR TISSUE: AN OVERVIEW

• The radiolucent area may be larger than a gran- • The mandibular posterior teeth are most fre- uloma and may include more than one tooth. quently affected.

Location 60% of cysts are found maxilla, especially Histopathology around incisors & canines. Microscopically, condensing osteitis appears as an Histopathology area of dense bone with trabecular borders lined Radicular cysts consist of a cavity lined with strat- with osteoblasts. Chronic inflammatory cells, plasma ified squamous epithelium derived from epithelial cells, and lymphocytes are seen in the scant bone cell rests of Malassez present in the periodontal liga- marrow. ment. Periradicular inflammatory changes cause the Treatment:Root canal treatment is a treatment of epithelium to proliferate. As the epithelium grows choice into a mass of cells, the center loses the source of Prognosis: Excellent, lesion may persist after en- nutrition from the peripheral tissues. These changes dodontic treatment produce necrosis in the center; a cavity is formed, Asymptomatic Apical Abcess (20, 24) and a cyst is created. A chronic alveolar abscess is a long standing, low- Treatment grade infection of the periradicular alveolar bone. The source of the infection is in the root canal. • Extraction if involved tooth Etiology • Root canal treatment Natural sequeale of death of the pulp with extension of the infective process periapically or it may result Condensing Osteitis/Chronic Focal Sclerosing Os- from a pre-existing acute abscess. teomyelitis (30) Symptoms Condensing Osteitis is the response to a low-grade, A tooth is generally asymptomatic, no response to chronic inflammation of the periradicular area as a pulp vitality test such an abscess is detected only dur- result of a mild irritation through the root canal. ing routine radiographic examination Continuously / Etiology intermittently draining sinus tract which may seen as Alveolar bone is stimulated by osteoblastic activity a stoma on the . from pulpal disease resulting in degeneration. Diagnosis

Symptoms • May be painless or only mildly painful. • At times, radiographic evidence of osseous • Tooth may be asymptomatic/ sensitive to stim- breakdown is seen during routine examination uli. or discoloration of the crown of the tooth.

• Vitality tests: the tooth may or may not respond • The radiograph often shows a diffuse area of bone rarefaction, but the radiographic appear- ance of the lesion is non diagnostic. Diagnosis • Thickening of PDL. The rarefied area may be so diffuse as to fade indistinctly into normal bone. • Radiographs shown localized area of radio- opacity surrounding the affected root. Histopathology • It is an area of dense bone with reduced trabec- As the infective process extends to the periapical ular pattern. tissues or as toxic products diffuse through the apical

CMRO 11 (10), 652−664 (2020) CURRENT MEDICAL RESEARCH AND OPINION 662 Singh G et al. CURRENT MEDICAL RESEARCH AND OPINION foramen. Some of the periodontal fibers at the root 4. Heyeraas KJ, Kvinnsland I. Tissue pressure apex are detached or lost, followed by destruction of and blood flow in pulpal inflammation. Proc Finn the apical periodontal ligament. The apical cemen- Dent Soc 1982;88 (Suppl 1): 393-401. tum may also become affected. Lymphocytes and plasma cells are generally found toward the periph- 5. Al Reader, Nusstein J, Hargreaves KM. ery of the abscessed area, with variable numbers of Local anesthesia in endodontics. Pathways of pulp. PMN’S at the center. Mononuclear cells may also be 9th ed. St.Louis, Missouri: Mosby/Elsevier 2006. present. Fibroblasts may start to form a capsule at the periphery. The root canal itself may appear to be 6. Ali SG, Mulay S. Pulpitis: A review. IOSR empty or cellular debris may be present. J Dent Med Sci 2015;14(8): 92-97. Treatment 7. TrowbridgeHO. Review of dental pain- Drainage must be established by either opening the Histology and Physiology. J Endod 1986;12(10): pulp chamber or extracting the tooth Root canal 445-52. therapy may be carried out. If not treated lead to – osteomyelitis, cellulitis, bacteremia, fistulous tract 8. Grossman LI. Endodontic Practice. 9th edn. formation opening on the skin. Philadelphia: Lea &Febiger, 1978:51-75.

9. mulsen MH, Sieraski SM. Histophysiology 3 SUMMARY AND CONCULSION and diseases of thedental pulp. In: Weine FS, ed. Endodontic therapy. 4th edn. St.Louis: Mosby, Pulp and periodontal tissue form basis of dental prac- 1989:128-150. tice. Patient mainly seek dental treatment because of pain and discomfort. So every dentist should have 10. Abbott PV, Yu C. A clinical classification proper knowledge of every disease related to pulp of the status of the pulp and the root canal system. and periodontal tissue on the basis of which proper Aus Dent J 2007;52(1 Suppl): S17-S31. diagnosis can be made on the basis of this diagnosis proper treatment plan can be made and implemented 11. Dabuleanu M. Pulpitis reversible/ for the well being of patients. irreversible. J Can Dent Assoc 2013;79: 90-94.

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